【摘要】 目的研究脂多糖(lipopolysaccharide,LPS)诱导的脑内炎性损害以及银杏内脂B(BN52021)的干预治疗效果。方法Sprague-Dawley大鼠30只,随机分为对照组,模型组和治疗组(BN52021治疗),每组10只。第Ⅳ脑室注射LPS造模,Morris水迷宫检测实验动物学习和记忆能力;透射电了显微镜观察海马神经元突触数量及亚细胞结构的变化;免疫组织化学法检测脑内OX-42在小胶质细胞内的表达。结果治疗组大鼠的水迷宫逃避潜伏期比模型组显著缩短,平台象限游泳距离百分比显著增加;治疗组大鼠海马神经元内质网和核糖体数量比模型组明显增加,突触数量则无明显变化;治疗组大鼠脑内的OX-42阳性小胶质细胞数量比模型组明显减少,染色灰度上升。结论LPS可诱导脑内炎性损害,血小板活化因子受体拮抗剂BN52021对LPS诱导的脑内炎性损害具有保护作用,提示血小板活化因子受体拮抗剂对以中枢炎症为病理特征的神经退行性变有治疗作用。更多还原

【Abstract】 Objective To investigate lipopolysaccharide(LPS)induced acute cerebral inflammatory damage and the thera- peutic effect of ginkgolide B(BN52021).Methods Thirty Sprague-Dawley rats were randomly divided into 3 groups(n=10 for each group):Control group,Model group and Treatment group(treated with BN52021).LPS were injected into the fourth ventricle of rat to make a neuroinflammatory murine model.Morris water maze was used to detect the learning and memory ability of rats;changes of synapse number and subcellular ultrastructures were observed under a transmission electron microscope;OX-42 positive microglia in the brain was detected by immunohistochemical method.Results The average escape latency in the Treatment group were significantly shortened than that in the Model group;and the percentage of swimming distance traveled in platform quadrant accounting lor total distance increased markedly.The rough endoplasmic reticulum and polyribosomes in the Treatment group were more than that in the Model group,but the number of synapses seemed to have no obvious change.The number of OX-42 positive microglia in the Treatment group decreased markedly than that in the Model group,and the grey density of OX-42-positive cells increased significantly. Conclusion LPS can induce inflammatory damages to the brain,but the damage could be antagonized by BN52021.Platelet activating factor receptor antagonist may offer an effective therapy for neurodegeneration diseases.更多还原